Thursday, January 28, 2010

One of my readers asks whether the renowned evolutionist Richard Dawkins has ever written on the subject of human races. Do they exist? And, if so, did this process of biological diversification stop a long time ago? Or did it actually accelerate when cultural evolution began to accelerate some ten thousand years ago?

Yes, he did address this subject six years ago in the essay “Race and Creation” (Dawkins, 2004). The essay starts off by acknowledging Richard Lewontin’s finding that human genes vary much more within races than between them. In fact, ‘races’ account for only 6 to 15% of all human genetic variation.

Yet this leads to an apparent paradox. According to Lewontin, the data tell us that any two human groups will overlap genetically to a high degree. Our eyes, however, tell a different story:

Well, suppose we took full-face photographs of 20 randomly chosen natives of each of the following countries: Japan, Uganda, Iceland, Sri Lanka, Papua New Guinea and Egypt. If we presented 120 people with all 120 photographs, my guess is that every single one of them would achieve 100 per cent success in sorting them into six different categories.

This paradox has been noticed by others. I remember one who claimed that ‘racism’ prevented us from seeing the genetic overlap between Danes and Congolese. Actually, the same overlap exists between many species that are nonetheless anatomically and behaviorally distinct (see previous post). It isn’t racism that creates the discrepancy between the data and our lying eyes. It’s just that most genes are weakly influenced by natural selection, especially the ‘structural genes’ that Lewontin and other population geneticists love to study. Such genes tell us very little about the strong selection pressures that have sculpted human differences in anatomy and many other traits.

It is fallacious to assume, as Lewontin did, that all genes contribute equally to real functional differences between populations, whether species or races. In fact, most genes have little selective value, being often little more than ‘junk DNA’. Even when a gene clearly is functionally significant, the difference between one allele and another may be like that between Coke and Pepsi. It is also fallacious to assume that genes with low selective value vary between populations in the same way as genes with high selective value. In fact, the more a gene has selective value, the likelier it will vary across a boundary between two different population, since such boundaries usually coincide with geographical/ecological barriers that separate different adaptive landscapes and, hence, different selection pressures.

Dawkins uses ‘Lewontin’s paradox’ to show that races do exist. But how relevant are they to recent human evolution? Hasn’t cultural evolution replaced genetic evolution in our species? On this point, Dawkins argues that the former has actually stimulated the latter. He draws an analogy with sympatric speciation in insects:

Some people think the initial separation has to be geographical, while others, especially entomologists, emphasise so-called sympatric speciation, meaning that the initial separation, whatever it is, is not geographical. Many herbivorous insects eat only one species of plant. They meet their mates and lay their eggs on the preferred plants. Their larvae then apparently “imprint” on the plant that they grow up eating, and they choose, when adult, the same species of plant to lay their own eggs.

… In the case of these insects, you can see that, in a single generation, gene flow with the parental type could be abruptly cut off. A new species is theoretically free to come into being without the need for geographical isolation. Or, another way of putting it, the difference between two kinds of food plant is, for these insects, equivalent to a mountain range or a river for other animals. I am suggesting that human culture—with its tendency to distinguish between in-groups and out-groups—also provides a special way in which gene flow can find itself blocked, which is somewhat analogous to the insect scenario I have just outlined above.

In the insect case, plant preferences are handed down from parent to offspring by the twin circumstances of larvae fixating on their food plant, and adults mating and laying eggs on the same food plants. In effect, lineages establish “traditions” that travel longitudinally down generations. Human traditions are similar, if more elaborate. Examples are languages, religions and social manners or conventions. Children usually adopt the language and the religion of their parents although, just as with the insects and the food plants, there are enough “mistakes” to make life interesting. Again, as with the insects mating in the vicinity of their preferred food plants, people tend to mate with others speaking the same language and praying to the same gods. So different languages and religions can play the role of food plants, or of mountain ranges in traditional geographical speciation. Different languages, religions and social customs can serve as barriers to gene flow. From here, according to the weak form of our theory, random genetic differences simply accumulate on opposite sides of a language or religion barrier, just as they might on opposite sides of a mountain range. Subsequently, according to the strong version of the theory, the genetic differences that build up are reinforced as people use conspicuous differences in appearance as additional labels of discrimination in mate choice, supplementing the cultural barriers that provided the original separation.

At this point, Dawkins winds up his essay, arguing that cultural differences in mate choice may explain many anatomical differences among human populations.

Fine. One point, though. Is mate choice the only human behavior that differs culturally? No, there are also differences in “languages, religions and social manners or conventions.” Wouldn’t these other differences generate selection pressures that likewise differ from one population to the next? And wouldn’t these selection pressures influence not only anatomy but also any trait with a substantial genetic component, including a wide range of behavioral predispositions, mental aptitudes, and personality factors? This would all follow logically from Dawkins’ reasoning. Indeed, he seems to hint at this when he states that “traditions” are no less part of our adaptive landscape than food plants. Having dropped the hint, he goes no further. End of essay.

It’s not as if I’m alone in making the above point. Claude Lévi-Strauss—hardly a rabid sociobiologist—brought it up in a lecture he gave in 1979:

The selection pressure of culture—the fact that it favors certain types of individuals rather than others through its forms of organization, its ideas of morality, and its aesthetic values—can do infinitely more to alter a gene pool than the gene pool can do to shape a culture, all the more so because a culture’s rate of change can certainly be much faster than the phenomena of genetic drift. (Lévi-Strauss, 1979, p. 24-25)

But Lévi-Strauss was never afraid to spell out what he thought. He was a public intellectual in the true sense of the word. In contrast, Richard Dawkins just hints, and hints, and hints … in the hope that someone else will pick up the ball and run with it.

Thursday, January 21, 2010

In a previous post, I noted certain discrepancies between Luca Cavalli-Sforza’s current stand on the race concept and his earlier one. This reversal seems to have occurred between his 1976 book Genetics, Evolution, and Man and his 1994 opus The History and Geography of Human Genes (whose cover map is curiously at odds with his statement that human genetic variation does not cluster into racial groups).

Such a change of heart is all the more puzzling because the case against the race concept had already been made in 1972, when Richard Lewontin showed that genetic differences within human races greatly exceed genetic differences between human races. That was—and still is—the main argument for race denialism. If this argument failed to convince Cavalli-Sforza in 1976, what happened to make it more convincing in 1994?

This is all the more puzzling because several authors since 1972 have challenged Lewontin’s argument. Mitton (1977) and (1978) showed that within-race variation exceeds between-race variation only if one gene is examined at a time. The pattern reverses if several genes are examined at the same time. Another flaw in Lewontin's argument is that he used genetic data from genes that code for enzymes, blood groups, and various building blocks of human tissue. Yet these ‘structural’ genes appear to have been marginal to human evolutionary change. As Stephen J. Gould (1977, p. 406) noted:

The most important event in evolutionary biology during the past decade has been the development of electrophoretic techniques for the routine measurement of genetic variation in natural populations. Yet this imposing edifice of new data and interpretation rests upon the shaky foundation of its concentration on structural genes alone. (faute de mieux, to be sure; it is notoriously difficult to measure differences in genes that vary only in the timing and amount of their products in ontogeny, while genes that code for stable proteins are easily assessed).

Indeed, if we look at differences in structural genes we see a high degree of overlap not only between human populations but also between morphologically distinct species (see previous post).

So why did Cavalli-Sforza change his mind? A cynical answer was provided to me by one anthropologist: “I don't think our perception of the general patterns of genetic variation changed much from '76 to '94, but the intellectual climate that geneticists operate in sure did.”

Some light has been shed on this question by Sesardic (2010). Aside from being an excellent rebuttal of race denialism, this paper also quotes an unpublished manuscript by one of Cavalli-Sforza’s collaborators A.W.F. Edwards. The manuscript describes the following episode:

When in the 1960s I started working on the problem of reconstructing the course of human evolution from data on the frequencies of blood-group genes my colleague Luca Cavalli-Sforza and I sometimes unconsciously used the word ‘race’ interchangeably with ‘population’ in our publications. In one popular account, I wrote naturally of ‘the present races of man’. Quite recently I quoted the passage in an Italian publication, so it needed translating. Sensitive to the modern misgivings over the use of the word ‘race’, Cavalli-Sforza suggested I change it to ‘population’. At first I was reluctant to do so on the grounds that quotations should be accurate and not altered to meet contemporary sensibilities. But he pointed out that, as the original author, I was the only person who could possibly object.

Thursday, January 14, 2010

Do empires provide a higher standard of living? In theory, this might seem so. Empires allow goods, capital, and labor to circulate within a much larger land area, thus creating economies of scale and matching supply and demand more efficiently. Empires can also build public works—roads, canals, aqueducts, etc.—that are beyond the reach of smaller territorial entities.

This is still the view in much scholarly writing on the Roman Empire. Yet it is inconsistent with what physical anthropologists are discovering through analysis of skeletal remains. The latest of these studies concerns child burials from 3rd to 5th century Roman Dorchester, in southern England. The children show high levels of malnutrition and trauma: 38.5% had cribra orbitalia—a sign of iron or vitamin B12 deficiency; 12.5% had rickets—a sign of vitamin D deficiency; 4.8% had scurvy—a sign of vitamin C deficiency; and 5.4% had broken ribs (Lewis, 2010).

These rates are much higher than those for medieval England and point to a very poor diet. The incidence of rickets is interesting, since we see a similar high prevalence in industrial England (18th – early 20th centuries). The latter rickets epidemic is usually attributed to industrial smog that blocked UVB radiation and thus impaired vitamin-D synthesis in the skin. A likelier culprit is a diet made up almost wholly of bread, whose high content of phytic acid increases vitamin-D requirements by binding to calcium and phosphorus in the body, thus making these elements unusable (Lindeberg, 1997). This is also probably the cause of Roman-era rickets.

Lewis (2010) cites similar findings from other Roman sites:

Many questions remain about what impact the introduction of urban centers and the gradual economic decline at the end of the Roman Empire had on the local population. Some Roman scholars argue that “Romanization” brought about improvements to the health of the people (Mattingly, 2006, p. 323), with the writing of Roman architects such as Vitruvius conjuring up images of planned Roman cities, with marbled surfaces and flowing water, providing extensive facilities for the comfort and health of the inhabitants (Morley, 2005). Diametrically opposed is the argument that urbanization widened the divide between the rich and the poor, with many suffering hardships of poverty, social unrest, and subservience to the conquering population. The city of Rome itself is seen as overcrowded and filthy, with dogs and muggers prowling the streets, whereas the archaeological evidence calls into question the organization of the water supply and levels of sanitation, with latrines discovered near kitchen areas (Laurence, 1997; Morley, 2005). Garnsey (1999) has hypothesized that undernutrition was endemic in the urban communities of the Greco-Roman world …

Although the Roman Empire brought about an increase in economic wealth, much of this increase seems to have been either siphoned off by the elite or consumed by the large standing army. There is very little evidence that the average citizens were better off under imperial rule, and much suggests that they were worse off.

Why? One reason may be ‘diseconomies of scale.’ Empires tend to liquidate smaller communal entities that more efficiently deliver collective goods, such as community policing, high-trust social networks (for exchange of services and sharing of scarce goods), and support for family formation and child care. This is particularly evident in the Roman Empire’s high infantile mortality rate and low birth rate, with the result that natural increase became negative in late imperial times.

These smaller communal entities were liquidated by the tendency of individuals to migrate from one part of the Empire to another, either on their own or through resettlement of legionnaire veterans. This process of liquidation was also assisted by the State itself, which saw private collectivities as sources of conspiracy or rebellion. In fact, only a limited number of non-State associations were allowed, such as guilds, burial clubs, and officially recognized religions. The persecution of Christians was part of this tendency to see smaller collectivities as threats to the Empire.

Many of us, living in countries where for several centuries we have had fair liberty of association, may not realize just how recent such freedom is but realize that a civilization in which states fear their own citizens is one that recognizes its own inhumanity. Thus it cannot surprise us that in Antiquity most noncommercial associations were forbidden: the authorities realized that any social club might be a center for opposition to the régime. (source)

Empires also make life worse for the average person by fostering dependence on long-distance economic relationships that may collapse if one link in the supply chain disappears. When barbarian invasion disrupted grain shipments between North Africa and Italy in the 5th century, urban populations were suddenly without food. In general, empires create relationships between people who have no commitment to each other beyond short-term economic interest. When a crisis happens, these same people will give priority to their kinfolk … thus leaving in the cold any atomized individuals with no kinship networks to fall back on. When the Roman Empire collapsed, the latter were the ones who suffered the most.

References

Lewis, M.E. (2010). Life and death in a civitas capital: metabolic disease and trauma in the children from late Roman Dorchester, Dorset, American Journal of Physical Anthropology, early view.

Thursday, January 7, 2010

Back in 2005, it was found that human populations vary considerably at two genes, ASPM and microcephalin, that control the growth of brain tissue. The finding seemed to be ‘huge’ in its implications. Then, it all fizzled out. No correlation could be found between variation at either gene and differences in mental ability or head circumference (Mekel-Bobrov et al., 2007; Rushton et al., 2007).

A recent study has now shown that ASPM and several other genes (MCPH1, CDK5RAP2, CENPJ) do in fact influence growth of brain tissue, specifically cortical tissue. Moreover, this influence seems to be strongest for the regulatory regions of these genes, i.e., the portions that regulate the behavior of other genes. But why did earlier studies fail to find anything? One reason is that the software at the time was not sophisticated enough to calculate cortical surface area (as opposed to overall brain volume). Another reason is that earlier studies focused on the non-regulatory regions of these genes.

In 2010, we’ll probably see further developments in this area. Stay tuned …

Early modern human genome

Scientists have retrieved mtDNA from a 30,000 year-old hunter-gatherer from Kostenki, Russia. This seems to be part of a trend to study the genome of early modern humans. The challenge now will be to reconstruct not only the mtDNA but also the nuclear DNA—a serious problem because contamination from contemporary human sources cannot easily be ruled out. Significantly, Prof. Paabo has discovered several ways to minimize contamination.

Population differences in vitamin D metabolism

This year will see further evidence that natural selection has caused differences in metabolism among different human populations, including vitamin D metabolism.

For instance, many populations have long been established at latitudes where vitamin-D synthesis is impossible for most of the year. Some of these populations can get vitamin D from dietary sources (e.g., fatty fish) but most cannot. In these circumstances, natural selection seems to have adjusted their metabolism to reduce their vitamin-D requirements. We know that the Inuit have compensated for lower production of vitamin D by converting more of this vitamin to its most active form (Rejnmark et al., 2004). They also seem to absorb calcium more efficiently, perhaps because of a different vitamin-D receptor genotype (Sellers et al., 2003). Even outside the Arctic zone, there seem to be differences in vitamin-D metabolism from one population to another. In particular, vitamin-D levels seem to be generally lower in darker-skinned populations (Frost, 2009).

These findings will force us to revisit the vitamin-D hypothesis of European skin color. According to this hypothesis, Europeans are white-skinned because their ancestors had to maintain the same level of vitamin-D synthesis at latitudes where UVB radiation is much weaker. This leaves unexplained the much darker skin of indigenous peoples at similar latitudes in northern Asia and North America. More importantly, it posits vitamin-D metabolism as a ‘given’ that human skin color has to adjust to, when in fact this metabolic pathway is just as amenable to natural selection as everything else.

There probably is a causal link between white skin and European vitamin-D metabolism, but the sequence of cause and effect may run in the opposite direction:

2. Because this depigmentation ensured abundant vitamin-D synthesis in the skin, there was a relaxation of selection pressure on vitamin-D metabolism. This would explain why, in comparison to other populations, Europeans convert less of it to its most active form and why it binds less effectively to the type of vitamin-D receptor that is most common among Europeans.

Unfortunately, our norms for adequate vitamin intake are based on subjects or populations of European origin. We are thus diagnosing vitamin-D deficiency in non-European individuals who are, in fact, perfectly normal. This is particularly true for African Americans, nearly half of whom are classified as vitamin-D deficient, even though few show signs of calcium deficiency—which would be a logical outcome. Indeed, this population has less osteoporosis, fewer fractures, and a higher bone mineral density than do Euro-Americans, who generally produce and ingest more vitamin D (Frost, 2009).

By pathologizing non-Europeans as being vitamin-D deficient, modern medicine is paving the way for programs that are well intentioned but ultimately tragic in their consequences: mass vitamin-D supplementation to be dispensed through the school system and awareness campaigns. Such public health programs have already been proposed for African Americans and northern indigenous peoples.

What will be the outcome of raising vitamin-D levels in these populations? Keep in mind that we are really talking about a hormone, not a vitamin. This hormone interacts with the chromosomes and gradually shortens their telomeres if concentrations are either too low or too high. Tuohimaa (2009) argues that optimal levels may lie in the range of 40-60 nmol/L. In non-European populations the range is probably lower. It may also be narrower in those of tropical origin, since their bodies have not adapted to the wide seasonal variation of non-tropical humans.

If this optimal range is continually exceeded, the long-term effects may look like those of aging:

Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan.

… after the Second World War in Europe especially in Germany and DDR, children received extremely high oral doses of vitamin D and suffered hypercalcemia, early aging, cardiovascular complications and early death suggesting that hypervitaminosis D can accelerate aging. (Tuohimaa 2009)

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Welcome to my blog! For the most part, this page will be an extension of my website, with comments relating to my research. But it will also branch out into more general discussions of human evolution.